MiR-1179 is downregulated in cervical cancer and its overexpression suppresses cancer cells invasion by targeting CHAF1A/ZEB1

  • Fahui Lv Department of Obstetrics and Gynaecology, The No.2 People’s Hospital of Hefei, Hefei, Anhui Province, 230011, China
  • Youwen Zhong School of Economics and Finance, School of Economics and Finance, Xi’an Jiaotong University, Xi’an, Shaanxi Province,710061, China
  • Ling Sang Department of Obstetrics and Gynaecology, The No.2 People’s Hospital of Hefei, Hefei, Anhui Province, 230011, China
  • Xiaoling Wu Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi Province, 710004, China https://orcid.org/0000-0002-5713-4937

Abstract

The anticancer effect of miR-1179 has been extensively studied in many tumors. The mechanism of miR-1179 action in cervical cancer, however, remains largely unknown. In the present study, miR-1179 was downregulated in both cervical cancer cell lines and cancer tissues. In addition, miR-1179 mimic suppressed cancer cells invasion and epithelial-mesenchymal transition (EMT) in cervical cancer SiHa and Caski cells. We found that chromatin assembly factor 1 subunit A (CHAF1A) might be a direct target of miR-1179 and could be regulated by miR-1179. Furthermore, CHAF1A shRNA suppressed the cervical cancer cells invasion and the expression of EMT-promoted proteins. Reversely, CHAF1A overexpression not only promoted cervical cancer cells invasion but also upregulated the level of Zinc finger E‐box binding protein 1 (ZEB1), an EMT-related protein. The induction of ZEB1 could be counteracted by miR-1179 overexpression. It was observed that in cervical cancer patients’ tissues, miR-1179 was downregulated while the pathway of CHAF1A/ZEB1 was upregulated. In summary, our research indicated that the miR-1179 might regulate CHAF1A/ZEB1 axis and inhibit the invasion of cervical cancer cells.

Published
2021-03-19
Section
Articles